Bowles D K, Laughlin M H, Sturek M
Vascular Biology Laboratory, Dalton Cardiovascular Research Center, and Departments of Physiology and Veterinary Biomedical Sciences, University of Missouri, Columbia, Missouri 65211, USA.
J Appl Physiol (1985). 1998 Apr;84(4):1225-33. doi: 10.1152/jappl.1998.84.4.1225.
The present study examined whether regulation of coronary tone in conduit arteries (>1.0 mm ID) is altered by exercise training. Yucatan miniature swine were treadmill trained for 16-20 wk (Ex) and compared with sedentary counterparts (Sed). Endothelium-denuded arterial rings were stretched to optimal length and allowed to equilibrate for 60 min. Inhibition of either Ca2+-activated channels [1 mM tetraethylammonium (TEA) or 10 nM iberiotoxin (IBTX)] or voltage-dependent K+ channels [1 mM 4-aminopyridine (4-AP)] significantly increased resting tension in both groups; however, the effect of all K+-channel blockers was greater in Ex. Addition of 1 mM sodium nitroprusside reduced resting tension in both groups, confirming the presence of active basal tone; however, sodium nitroprusside-sensitive tone was increased approximately twofold in Ex compared with Sed group. Perforated patch-clamp experiments on isolated smooth muscle cells demonstrated no effect of exercise training on whole cell TEA-sensitive, 4-AP-sensitive, or basal K+ current. Similarly, whereas TEA, 4-AP, and IBTX all decreased resting membrane potential, there was no difference in depolarization between groups. The greater effect of TEA on resting tension in Ex could be mimicked in Sed by addition of the Ca2+-channel agonist BAY K 8644. In conclusion, the greater response to K+-channel blockers after exercise training is consistent with an increased contribution of K+ channels to regulation of basal tone in conduit coronary arteries. The lack of an effect of training on K+ current characteristics or membrane potential responses in isolated cells suggests that a requisite factor for enhanced K+-channel activation in arteries from Ex, possibly stretch, is absent in isolated cells.
本研究探讨了运动训练是否会改变传导动脉（内径>1.0 mm）中冠状动脉张力的调节。尤卡坦小型猪在跑步机上训练16 - 20周（Ex组），并与久坐不动的对照组（Sed组）进行比较。将去内皮的动脉环拉伸至最佳长度，并使其平衡60分钟。抑制钙激活通道[1 mM四乙铵（TEA）或10 nM埃博毒素（IBTX）]或电压依赖性钾通道[1 mM 4 - 氨基吡啶（4 - AP）]均显著增加了两组的静息张力；然而，所有钾通道阻滞剂对Ex组的作用更大。添加1 mM硝普钠可降低两组的静息张力，证实存在活性基础张力；然而，与Sed组相比，Ex组中硝普钠敏感的张力增加了约两倍。对分离的平滑肌细胞进行穿孔膜片钳实验表明，运动训练对全细胞TEA敏感、4 - AP敏感或基础钾电流没有影响。同样，虽然TEA、4 - AP和IBTX均降低了静息膜电位，但两组之间的去极化没有差异。通过添加钙通道激动剂BAY K 8644，Sed组中TEA对静息张力的更大作用可被模拟。总之，运动训练后对钾通道阻滞剂的更大反应与钾通道对传导冠状动脉基础张力调节的贡献增加一致。训练对分离细胞中钾电流特性或膜电位反应没有影响，这表明在分离细胞中不存在Ex组动脉中增强钾通道激活的必要因素，可能是拉伸。
